Silica induces nuclear factor-kappaB activation through TAK1 and NIK in Rat2 cell line.

Silica has been known to be a factor in acute cell injury and chronic pulmonary fibrosis. In Rat2 fibroblasts, silica induced the activation of nuclear factor-kappa B (NF-kappaB), which plays a crucial role in regulating the expression of many genes involved in the subsequent inflammatory response. In addition, we observed that transforming growth factor-beta activated kinase 1 (TAK1) and NF-kappaB-inducing kinase (NIK) were involved in silica-mediated NF-kappaB activation in Rat2 cells.

Tumor necrosis factor-alpha gene promoter polymorphism in coal workers' pneumoconiosis.

Tumor necrosis factor-alpha (TNF-alpha) is believed to play a central role in the pathogenesis of pneumoconiosis. TNF2, a polymorphism in the TNF-a gene promoter, has been associated with an increase in TNF-alpha production and airway inflammation. To investigate the frequency of TNF2 in patients who have coal workers' pneumoconiosis (CWP) and to determine whether it is associated with development of a large opacity in CWP, we investigated the expression ofthe TNF2 allele in 80 patients who had CWP and in 54 healthy controls using restriction fragment length polymorphism (RFLP).